Abstract：
Apoptotic pore formation in mitochondria is the pivotal point for cell death during mitochondrial apoptosis. It is regulated by BCL-2 family proteins in response to various cellular stress triggers and mediates mitochondrial outer membrane permeabilization (MOMP). This allows the release of mitochondrial contents into the cytosol, which triggers rapid cell death and clearance through the activation of caspases. However, under conditions of low caspase activity, the mitochondrial contents released into the cytosol through apoptotic pores serve as inflammatory signals and activate various inflammatory responses. In this chapter, we discuss how the formation of the apoptotic pore is regulated by BCL-2 proteins as well as other cellular or mitochondrial proteins and membrane lipids. Moreover, we highlight the importance of sublethal MOMP in the regulation of mitochondrial-activated inflammation and discuss its physiological consequences in the context of pathogen infection and disease and how it can potentially be exploited therapeutically, for example to improve cancer treatment.
摘要：
线粒体中凋亡孔的形成是线粒体凋亡过程中细胞死亡的关键点。它由BCL-2家族蛋白调节，以响应各种细胞应激触发因素，并介导线粒体外膜透化（MOMP）。这允许线粒体内容物释放到细胞质中，通过caspases的激活触发细胞快速死亡和清除。然而,在低caspase活性的条件下，通过凋亡孔释放到细胞质中的线粒体内容物充当炎症信号并激活各种炎症反应。在这一章中,我们讨论了BCL-2蛋白以及其他细胞或线粒体蛋白和膜脂如何调节凋亡孔的形成。此外，我们强调亚致死MOMP在调节线粒体激活的炎症中的重要性，并讨论其在病原体感染和疾病的背景下的生理后果，以及它如何潜在地被利用治疗，例如改善癌症治疗。
